Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We measured plasma atrial natriuretic factor levels and atrial natriuretic factor secretion by isolated left atria from aging rats to determine the secretory response to stretch and adrenergic stimulation. Systolic arterial pressure and right atrial pressure were measured in vivo. Twenty-four hours later, atria were removed and studied in vitro in a perifusion system. After removal, stabilization at 0.7 g tension, and equilibration for 65 minutes, atria were stretched by increasing external tension for 20 minutes. After reequilibration atria were perifused with phenylephrine, 10(-5) M, for an additional 30 minutes. Right atrial pressure was not different between young (3 months) and aged (16-24 months) rats. Aged rats had higher plasma atrial natriuretic factor levels (52 +/- 8 versus 21 +/- 6 pmol/l; p less than 0.05) than young rats. Basal atrial natriuretic factor secretory rate in vitro was greater in atria from aged rats than young rats (875 +/- 35 versus 402 +/- 22 pg/min; p less than 0.05). Atria from aged rats had an increased response to phenylephrine compared with young rats (1,687 +/- 143 versus 788 +/- 113 pg/min; p less than 0.05) when means were adjusted for basal secretory rate. The secretory response to stretch was less than that of young rats (673 +/- 37 versus 773 +/- 27 pg/min), although this difference was not significant (p = 0.07). Atrial natriuretic factor secretion in response to adrenergic stimulation is increased with aging, and these secretory responses may contribute to increased plasma levels that occur during aging. In contrast to increased adrenergic responses, atrial natriuretic factor secretion after external stretch is not increased in aging rats.
Hypertension 1992 Jul
PMID:Alterations in the secretion of atrial natriuretic factor in atria from aged rats. 153 14

In this study we investigated the presence and anatomical location of atrial natriuretic factor (ANF) receptor subtypes in the rat central nervous system using in vitro autoradiographic and cross-linking techniques. 125I-ANF-(Ser99-Tyr126) served as a labeled ligand, whereas ANF-(Ser99-Tyr126) and two peptides endowed with selectivity for ANF-C receptor--namely, C-ANF (des-[Gln116-Gly120] ANF-[Asp102-Cys121]-NH2) and ANF-(Phe106-Ile113)-NH2--were used as displacing agents. Distribution studies revealed the presence of specific ANF binding sites in a number of central nervous system areas examined. C-ANF at 10(-6) M competed for 125I-ANF binding to a much lower extent than ANF in many of those structures, whereas ANF-(106-113)-NH2 at 10(-6) M did not have a significant effect on the radioligand binding except in the choroid plexus, pia-arachnoid, and olfactory bulb. Analysis of the competition curves revealed that in the choroid plexus, pia-arachnoid, olfactory bulb, subfornical organ, area postrema, and habenular nucleus, ANF interacts with its binding sites with high affinity (IC50, 0.46-0.77 nM). In contrast, C-ANF and ANF-(106-113)-NH2 competed for 125I-ANF binding with high potency (IC50, 2-16 nM) in the choroid plexus and pia-arachnoid only, where they were able to displace 60-70% of the radioligand binding. 125I-ANF cross-linking to olfactory bulb membranes resolved a specific 120-kDa band corresponding to the high molecular weight receptor but did not disclose a specifically labeled band corresponding to the low molecular mass receptor.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Jun
PMID:Atrial natriuretic factor receptor subtypes in the rat central nervous system. 164 66

To evaluate the existence of a relationship between atrial natriuretic factor (ANF) and plasma Na+/K+ATPase inhibitory activity in humans, we examined the hemodynamic and humoral response to volume expansion in 41 borderline hypertensive patients (BHT) with either normal (n = 33) or low plasma renin activity (n = 8). The study was carried out by measuring blood pressure, forearm circulation, plasma renin activity (PRA), ANF, and plasma levels of an endogenous Na+/K+ATPase inhibitor before and after 2 h of acute intravenous NaCl infusion (0.22 mL/min/kg bodyweight). The early (45 min) changes of ANF and those of Na+/K+ATPase inhibitory activity attained at the end of saline infusion were inversely related in BHT with normal PRA and directly related in the low-PRA population (r = 0.64). The time-course of ANF response to sodium loading was significantly delayed in BHT characterized by normal venous distensibility. They also showed a greater increase in plasma Na+/K+ATPase inhibitory activity occurring with an hypertensive, vasoconstrictive, and sodium retaining response as well. We conclude that in normal PRA borderline hypertensives, ANF may modulate the release of a plasma Na+/K+ATPase inhibitor in a setting where extracellular volume is acutely expanded. Our findings also suggest that dissimilarities in peripheral venous distensibility are able to influence the time-course of ANF response. The blunted ANF increase observed in response to NaCl loading in a subset of BHT could represent an early marker of the attitude of such patients to develop high blood pressure leading to the release of a Na(+)-pump inhibitor and influencing individual salt-sensitivity.
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PMID:Atrial natriuretic factor modulates the plasma levels of a Na+/K+ATPase inhibitor in volume expanded borderline hypertensives. 165 40

This study evaluates the release of atrial natriuretic factor (ANF) during maximal exercise in 7 patients with untreated moderate to severe hypertension with invasive monitoring of hemodynamic characteristics in relation to sympathetic activity. Peripheral venous ANF (fmol/ml) was determined at rest and maximal exercise producing a respiratory exchange ratio of 1.14 +/- 0.10. In 5 of 7 patients, simultaneous right ventricular and peripheral venous ANF samples could be obtained to assess exercise myocardial secretion of ANF. With exercise, mean blood pressure increased from 150 +/- 26 to 192 +/- 29 mm Hg (p less than 0.001), pulmonary wedge pressure increased from 7 +/- 3 to 18 +/- 10 mm Hg (p less than 0.05) and ANF increased from 11.7 +/- 8.2 to 25.7 +/- 15.9 (p less than 0.02). This ANF response correlated weakly with pulmonary wedge pressure (r = 0.497, p = not significant), since patients without an increase in pulmonary wedge pressure had no increase in ANF. However, changes in pulmonary wedge pressure and plasma norepinephrine during exercise were inversely correlated (r = -0.811, p less than 0.02), with the greatest increase in norepinephrine occurring with a minimal increase in pulmonary wedge pressure. Similarly, ANF and plasma norepinephrine were inversely correlated during exercise (r = -0.869, p less than 0.05). A significant increase in right ventricular ANF indicated myocardial secretion. Plasma ANF therefore increased because of active myocardial production during exercise in patients with moderate to severe hypertension. These findings further suggest a directionally opposing relation between ANF release resulting from increased atrial tension and sympathetic nervous system influence on cardiac performance during exercise.
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PMID:Exercise-induced secretion of atrial natriuretic factor and its relation to hemodynamic and sympathetic stimulation in untreated essential hypertension. 165 23

The vasodilator potency of human atrial natriuretic factor-(99-126) was investigated in the forearm vascular bed of 10 young and 10 elderly normotensive volunteers with venous occlusion strain gauge plethysmography. Atrial natriuretic factor was infused at six increasing dose steps into the brachial artery from 0.001 up to 0.3 microgram/min/100 ml of forearm volume. This induced a mean +/- SEM increase in blood flow from 1.4 +/- 0.2 up to 6.0 +/- 1.0 ml/min/100 ml in the young and from 1.4 +/- 0.2 up to 3.9 +/- 0.6 ml/min/100 ml in the elderly. The dose-response curves of forearm blood flow and of forearm vascular resistance after increasing infusion rates of atrial natriuretic factor were shifted to the right in the elderly when compared with the young subjects. The mean percent decrease in forearm vascular resistance, induced by atrial natriuretic factor, during this dose-response curve averaged -31 +/- 3% in the elderly versus -56 +/- 3% in the young subjects (p = 0.0002). The calculated forearm spillover of the second messenger of atrial natriuretic factor, cyclic guanosine monophosphate, significantly increased from baseline values of 1.2 +/- 1.1 and 0.7 +/- 0.5 pmol/min/100 ml in young and elderly subjects, respectively, up to 23.2 +/- 5.0 and 30.5 +/- 7.0 pmol/min/100 ml during the highest dose of atrial natriuretic factor (both p less than 0.01 versus baseline). There were no significant differences in the increments of the forearm spillover of this second messenger between both age groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Nov
PMID:Attenuated forearm vasodilator response to atrial natriuretic factor in the elderly. 165 70

Five weeks of high (8%) sodium intake, resulting in a decline of plasma atrial natriuretic factor (ANF) in normotensive Wistar-Kyoto (WKY) and Wistar rats, did not affect plasma ANF in spontaneously hypertensive rats (SHR) which became severely hypertensive. Regardless of salt consumption, SHR presented more pronounced glomerular particulate guanylate cyclase activation after large ANF doses in vitro than normotensive rats. In response to salt loading, plasma renin activity (PRA) and plasma aldosterone unexpectedly increased in SHR, in contrast to their decrease in the normotensive strains. Thus, SHR fail to react to prolonged high-salt intake as do normotensive rats, i.e. by a fall in plasma ANF, PRA and plasma aldosterone, and have higher stimulated glomerular particulate guanylate cyclase activity. Thus, ANF and its target response in SHR, as well as the PRA-plasma aldosterone reaction to prolonged salt loading, are distinct from those in normotensive strains. Since the relatively increased ANF and its target action in SHR appear to be a reactive antihypertensive defense rather than a primary event, systems other than ANF probably play an important role in the high salt-induced accelerated hypertension of SHR.
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PMID:Distinct plasma atrial natriuretic factor, renin and aldosterone responses to prolonged high-salt intake in hypertensive and normotensive rats. 167 17

Primary cultures of neonatal rat cardiocytes were exposed for 24 hours to culture media containing 0-2.0 mM extracellular calcium. Both atrial natriuretic factor (ANF) messenger RNA (mRNA) and ANF secretion were increased approximately threefold in the presence of 2.0 mM CaCl2 (vs. Ca2(+)-free medium). When cardiocytes were treated with the calcium channel blockers diltiazem, nifedipine, or verapamil, both ANF synthesis and secretion fell to 25-40% of control values. The choice of transcription start site on the ANF gene was not altered by the calcium channel blockers. When exogenous calcium was added to cardiocytes treated with verapamil, secretion of ANF was partially restored to control levels. High-performance liquid chromatographic analysis of medium from cardiocytes exposed to varying extracellular calcium concentrations or treated with calcium channel blockers for 24 hours revealed that the majority of secreted immunoreactivity (60-70%) migrated with pro-ANF (17 kDa) and that none of the various experimental manipulations significantly changed the ratio of pro-ANF to ANF in the media. These results were confirmed by immunoprecipitation analysis of the culture medium from the individual treatment groups. Treatment of cardiocytes for 24 hours with either the calcium ionophore A23187 or the phorbol ester 12-O-tetradecanoylphorbol 13-acetate increased ANF secretion. The combined use of these agents resulted in stimulation of both ANF secretion and ANF mRNA accumulation.
Hypertension 1990 Jan
PMID:Extracellular calcium regulates expression of the gene for atrial natriuretic factor. 168 46

Treatment of severe hypertension is beneficial, but reversibility of target-organ damage has not been characterized. Serial studies were performed in 15 patients with severe essential hypertension (age of 56 +/- 3 years, mean +/- SEM) treated for 1 year with 60 to 150 mg/day of continuous-release nifedipine; 3 patients required 50 mg of chlorthalidone/day to lower diastolic blood pressure (BP) to less than 95 mm Hg. Left ventricular (LV) structure and function was evaluated with two-dimensional-directed M-mode echocardiography, digitized from videotape and analyzed blindly. BP was markedly reduced from 194 +/- 8/115 +/- 4 to 146 +/- 4/88 +/- 14 mm Hg (p less than 0.0001) and maintained at this level for 1 year. Posterior wall and septal LV thickness, elevated at entry (12.9 +/- 0.1 and 13.4 +/- 0.1 mm), dropped steadily over 1 year into the normal range (10.0 +/- 0.03 and 11.2 +/- 0.1 mm, p less than 0.001). LV mass index, above 95% for normals at entry, decreased by 19% at 6 months (129 +/- 10 to 104 +/- 7 g/m2, p less than 0.01), and remained at this level at 1 year. LV fractional shortening rose steadily over 1 year from 34 to 42% (p less than 0.02). Atrial natriuretic peptide, which reflects LV filling pressures, was markedly elevated at entry, but was significantly reduced by 6 months (76 +/- 22 vs. 45 +/- 14 pg/ml, p less than 0.05). Sustained reduction of arterial BP with continuous-release nifedipine for 1 year normalizes LV mass, improves LV systolic function, and reduces circulating levels of atrial natriuretic peptide.
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PMID:Effect of nifedipine GITS on left ventricular mass and diastolic function in severe hypertension. 171 75

Arterial hypertension is found in as many as 75% patients with autosomal dominant polycystic kidneys with normal renal function, its pathogenesis is however not quite clear so far. The authors examined 16 patients with polycystic kidneys with normal or only slightly reduced renal function (plasma creatinine lower than 140 umol/l), 8 of these patients were normotonic (N) and 8 hypertonic (H). In all examined subjects right-sided cardiac catheterization was performed with assessment of the minute cardiac volume by thermodilution. To all patients in the course of one hour 1500 ml saline per 70 kg body weight were administered and the haemodynamic examinations were repeated after termination of the infusion. In all subjects before and after expansion the plasma renin activity was assessed (PRA), as well as plasma aldosterone (PA), plasma catecholamines (PC) and the atrial natriuretic factor (ANF), the renal blood flow and glomerular filtration by means of clearance and extraction of PAH and inulin clearance. The authors did not find differences in plasma concentrations, cardiac output and splanchnic and renal ANF extraction in groups N and H, nor in PRA, PA and PC. Volume expansion led in both groups to a comparable rise of ANF and suppression of PRA and PA. Group H did not differ from group N in any of the investigated haemodynamic and renal parameters except for systemic vascular resistance. In hypertensive patients before expansion a close correlation was found between pressure in the pulmonary artery in a wedged position and diuresis (r = 0.935, p less than 0.01) and natriuresis (r = 0.895, p less than 0.01). The volume expansion was in both groups associated with a comparable rise of diuresis, the haemodynamic response of patients N and H was however quite different. While in patients of group N a decline of the systemic vascular resistance occurred as well as an increase of the minute volume without a change of the renal flow and glomerular filtration, in hypertonic patients the systemic vascular resistance and minute volume did not change but there was a significant rise of the renal flow and glomerular filtration. The relationship of diuresis and natriuresis of hypertensive patients with polycystic kidneys to volume parameters and the rise of the renal perfusion pressure during volume expansion indicates the importance of pressure natriuresis for ensuring the sodium and volume homeostasis in these patients.
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PMID:[Hypertension in patients with polycystic kidneys--the effect of volume expansion]. 182 66

The cause of primary (essential) hypertension remains unknown, but a number of circulating hormones and endothelium-derived factors are probably involved. This review summarizes recent evidence on the roles of hyperinsulinemia, the renin-angiotensin system, atrial natriuretic factor, and three endothelium-derived factors--prostacyclin, endothelium-derived relaxing factor, and endothelin.
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PMID:Hormonal and local factors in hypertension. 182 31


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